We are studying control of expression of globin genes by using as a model system, the K562 human leukemia cell line. We previously showed that these primitive cells can be reversibly induced by hemin to accumulate large amounts of embryonic fetal hemoglobins in the absence of erythroid differentiation. Hybridization of nick-translated 32P-globin cDNA probes to agarose gel blots of RNA showed increased globin mRNA levels in induced cells. Quantitation by isolation and in vitro translation of mRNA for the Alpha, Gamma, Espilon, and Lambda globins expressed in these cells has shown several-fold chain specific increases after induction. This suggests that at least part of the effect of hemin is exerted at the transcriptional level. No evidence of Beta-globin production by K562 cells has been obtained which indicates the line may be developmentally arrested at an embryonic or fetal level. Preliminary data suggest that this lack of expression is not due to hypermethylation of Beta-globin DNA.